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t/f viruses are alive
trick question- they are obligate intracellular organisms whose life cycle is intimately tied to that of its host cell, they cannot make energy or macromolecules (DNA/RNA/proteins) independently of the eukaryotic host cell
why is virology relevant to dentistry?
dental infection control
patient screening, personal hygiene, personal protection, instrument processing, surface asepsis, patient treatment, laboratory disinfection
what are the various methods of classifying viruses and what are the classifications within that type?
type of nucleic acid genome: DNA or RNA / type of strand and their polarity / segmented or one piece
capsid: icosahedral or helical or complex / enveloped or non-enveloped
replication strategy
genome sequence similarity
symptoms: hepatitis virus, respiratory virus, encephalitis virus
tropism: neurotropic, ect
mode of transmission: arboviruses
host: plant viruses, animal viruses, bacteriophage
virion
complete virus particle
nucleic acid core
DNA or RNA, nucleoproteins
protein coat
capsid, nucleocapsid, spikes/viral attachment proteins (VAPs)
virion
a virus particle, nanometers (nm) are unit of measurement
what is the clinically important range for viruses?
18nm - 300 nm
capsid
single or double layer protein shell surrounding the viral nucleic acid, composed of subunits (protomer and capsomer) arranged in a symmetric pattern
nucleocapsid
nucleic acid + capsid
each capsid subunit has the capacity to…
bind to other subunits in specific ways, these physical interactions between subunits permits self assembly to form virus capsid (virions)
spikes / viral attachment proteins
surface structures that mediate the interaction of the virus with the target cell, removal or disruption inactivates the virus, antibodies generated against it prevent virus infection
enveloped virus
lipid bi-layer envelope, protein projections like glycoproteins or VAPs, is essential for infectivity
naked capsid characteristics
stable, released by cell lysis, transmission: easily spread, fomites, longer survival time, may survive gut
enveloped virus characteristics
labile, released by budding or cell lysis, transmission: must remain wet, close contact or droplets, destroyed in gut
what are some structures of capsids
icosahedral, helical, complex
helical symmetry
example is TMV, non-enveloped, capsid: RNA helix with associated nucleoproteins
icosahedral symmetry
repeating subunits (few proteins), subunits can self assemble, efficient (largest volume possible), very strong
T4 bacteriophage
both helical and icosahedral structure
complex virus structures
general principles of symmetry are often used to build part of the virus shell but it cannot be simply defined by a mathematical equation
poxvirus
complex symmetry
DNA in viruses
stable molecule, larger (3-300kbp), dsDNA (circular and linear), pdsDNA (partially double/single stranded circular DNA), ssDNA (linear)
RNA in viruses
easily degraded, smaller (3-30kbp), dsRNA (segment), +ssRNA, -ssRNA, -ssRNA segmented, +_ ambisense
t/f the viral genome contains all the information needed to direct the host cell to synthesize virus encoded proteins but they are dependent on the host cell for substrates, energy, and machinery required for protein and nucleic acid synthesis
true
t/f in most cases, host cells mcaromolecular synthesis is not shut down, the host cells just make their proteins along with viral proteins
false- most of the time viruses shut down host cell macromolecular synthesis
what are the general steps of the replication cycle of all viruses
adsorption or attachment
penetration
uncoating and eclipse
transcription
synthesis of viral components
assembly
release of virions
what steps may overlap?
penetration and uncoating
where do critical events of viral replication occur?
cell nucleus or exclusively within the cytoplasm
how long is the period between infection and the production of the new virion?
can be as short as 3 hrs or as long as several months to years
adsorption or attachment
VAPs mediate recognition and attachment of the virus to receptors on host cells
host range, cell, and tropism may be restricted by specificity of VAP for host cell receptors expressed only on certain cell types
penetration
use the same pathways used by cells to take up macromolecules
non-enveloped: receptor mediated endocytosis (virion is taken up into endosomes) or viropexis (virion penetrates plasma membrane directly)
enveloped: fusion and release the nucleocapsid or genome into the cytoplasm, viral proteins mediate fusion with cellular membranes
uncoating and eclipse
period where no intact infectious virus can be detected, begins with uncoating of lipid membrane and protein capsid surrounding the nucleic acid viral core, as uncoating proceeds the viral nucleic acid becomes free to act as a template for synthesis of virus RNA
transcription
virus mRNA codes for synthesis of enzymes necessary to complete the process of uncoating itself and also initiate early steps in viral replication
during this, the synthesis of host cell RNA is halted so host ribosomes are free to receive viral mRNA and provide a focus for transcription and synthesis of viral proteins
structural viral proteins
proteins that make up the virus particle, synthesized on cellular polyribosomes
non-structural viral proteins
enzyme required for virus genome replication
t/f during synthesis of viral components, there is a simultaneous synthesis of progeny viral nucleic acid using synthesized nucleic acid polymerases
true
assembly
accomplished by incorporation of viral nucleic acid into putative capsomeres: procapsids, may occur in the cell nucleus, cytoplasm, or at the plasma membrane (enveloped viruses)
release of virions
may occur either through gradual budding (enveloped viruses) or sudden rupture
viral genetics
mutations and the effects on viral replication and pathogenesis, interactions of 2 genetically different viruses when they co-infect the same cell
wild type / parental virus
the original virus from which mutants or variants are derived / compared to
may not be the same as the virus found in nature
what are the types of mutations?
spontaneous or induced
lethal mutation
mutations in essential genes, virus cannot replicate
attenuated mutations
mutations that result in less virulent virus strains or variants, often developed and used as vaccine strains
revertant mutant
mutation that results in a change from a mutant genotype to the wild type genotype
defective viruses
lack 1 or more functional genes required for virus production and require helper activity from another virus
some require unrelated helper viruses
recombination
interaction among viruses that results in progeny that have phenotypic and genotypic differences from either parent, typically occurs via nucleic acid strand breakage and recombination between parental genomes
reassortment
interaction among viruses that can occur with viruses with segmented genomes when 2 different virus strains co-infect a cell, packaging of gene segments from the different parental strains in progeny may result in new virus phenotype
complementation
interaction of viral gene products in cell infected with 2 viruses, 1 or both defective
allows replication of 1 or both viruses under normally non-permissive conditions
genotypes are unchanged
results from 1 virus providing gene product that is defective in the other virus
if both viruses are defective in the same gene, no complementation
phenotypic mixing / transcapsidation
can occur when cells co-infect with different virus strains and progeny virions are produced that have the genome from one strain, but the capsid proteins from the other strain